Instituto de Biomedicina de Sevilla (IBIS), Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Consejo Superior de Investigaciones Científicas, Sevilla, Spain.
CIBER de Cancer, IS Carlos III, Madrid, Spain.
Cell Death Dis. 2021 May 20;12(6):515. doi: 10.1038/s41419-021-03801-w.
The EMX (Empty Spiracles Homeobox) genes EMX1 and EMX2 are two homeodomain gene members of the EMX family of transcription factors involved in the regulation of various biological processes, such as cell proliferation, migration, and differentiation, during brain development and neural crest migration. They play a role in the specification of positional identity, the proliferation of neural stem cells, and the differentiation of certain neuronal cell phenotypes. In general, they act as transcription factors in early embryogenesis and neuroembryogenesis from metazoans to higher vertebrates. The EMX1 and EMX2's potential as tumor suppressor genes has been suggested in some cancers. Our work showed that EMX1/EMX2 act as tumor suppressors in sarcomas by repressing the activity of stem cell regulatory genes (OCT4, SOX2, KLF4, MYC, NANOG, NES, and PROM1). EMX protein downregulation, therefore, induced the malignance and stemness of cells both in vitro and in vivo. In murine knockout (KO) models lacking Emx genes, 3MC-induced sarcomas were more aggressive and infiltrative, had a greater capacity for tumor self-renewal, and had higher stem cell gene expression and nestin expression than those in wild-type models. These results showing that EMX genes acted as stemness regulators were reproduced in different subtypes of sarcoma. Therefore, it is possible that the EMX genes could have a generalized behavior regulating proliferation of neural crest-derived progenitors. Together, these results indicate that the EMX1 and EMX2 genes negatively regulate these tumor-altering populations or cancer stem cells, acting as tumor suppressors in sarcoma.
EMX(空泡螺旋框)基因 EMX1 和 EMX2 是参与大脑发育和神经嵴迁移过程中各种生物过程(如细胞增殖、迁移和分化)调节的 EMX 家族转录因子的两个同源域基因成员。它们在位置身份的指定、神经干细胞的增殖和某些神经元细胞表型的分化中发挥作用。总的来说,它们在从后生动物到高等脊椎动物的早期胚胎发生和神经胚发生中作为转录因子发挥作用。在一些癌症中,已经提出了 EMX1 和 EMX2 作为肿瘤抑制基因的潜力。我们的工作表明,EMX1/EMX2 通过抑制干细胞调节基因(OCT4、SOX2、KLF4、MYC、NANOG、NES 和 PROM1)的活性,在肉瘤中作为肿瘤抑制因子发挥作用。因此,EMX 蛋白下调在体外和体内均诱导了细胞的恶性和干细胞特性。在缺乏 Emx 基因的小鼠敲除(KO)模型中,3MC 诱导的肉瘤更具侵袭性和浸润性,具有更大的肿瘤自我更新能力,并且具有更高的干细胞基因表达和巢蛋白表达,高于野生型模型。这些表明 EMX 基因作为干细胞调节因子发挥作用的结果在不同亚型的肉瘤中得到了重现。因此,EMX 基因可能具有普遍的行为,调节神经嵴衍生祖细胞的增殖。总之,这些结果表明 EMX1 和 EMX2 基因负向调节这些改变肿瘤的群体或癌症干细胞,在肉瘤中作为肿瘤抑制因子发挥作用。